slide1 n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Non-Spore-Forming Gram-Positive Bacilli PowerPoint Presentation
Download Presentation
Non-Spore-Forming Gram-Positive Bacilli

Loading in 2 Seconds...

play fullscreen
1 / 83

Non-Spore-Forming Gram-Positive Bacilli - PowerPoint PPT Presentation


  • 582 Views
  • Uploaded on

Non-Spore-Forming Gram-Positive Bacilli. Corynebacterium C. diphtheriae Disease Diphteria Opportunistic infections by other Corynebacterium species (dipheroids). Properties. Club-shaped also V- or L-shaped Beaded appearance Methachromatic granules (Albert staining) Nonmotile

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Non-Spore-Forming Gram-Positive Bacilli' - althea-kelly


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
non spore forming gram positive bacilli
Non-Spore-Forming Gram-Positive Bacilli
  • Corynebacterium

C. diphtheriae

Disease

Diphteria

Opportunistic infections by other Corynebacterium species (dipheroids)

properties
Properties
  • Club-shaped also V- or L-shaped
  • Beaded appearance
  • Methachromatic granules (Albert staining)
  • Nonmotile
  • no capsule
  • Facultative anaerobic.
  • Classified in CNM group.
biotypes based on colony shape biochemical properties and virulence
Biotypes(based on colony shape, biochemical properties and virulence)

Gravis

Mitis

Intermedius

Belfanti

clinical finding
Clinical finding
  • Common diphtheria (Nasopharyngitis)

Incubation period of 2–5 days.

Fibrinousexudate “pseudomembrane”

Sore throat, fever, Enlargement of neck lymph nodes and neck edema. Irregulatory of cardiac rhythm, difficulties with vision, speech and swallowing.

Corrosion of myelin sheaths in the central and peripheral nervous system leading to degenerating motor control

clinical finding1
Clinical finding
  • Cutanous diphtheria

(a secondary infection)

  • Antibody production: Blocking the fragment B and so preventing entry into the cell.
transmission
Transmission
  • Humans the only natural host
  • C. diphtheriae reside in the upper respiratory tract
  • Transmitted by airborn droplet
  • Infection at the site of a pre-existing skin lesion
pathogenesis
Pathogenesis
  • Invasivness
  • Exotoxin
invasivness
Invasivness
  • Cord factor

A glycolipid inhibits eukaryotic cell oxidation.

  • Nuraminidase

Removes N-acetyl nuraminic acid from musine membranes.

exotoxin encoded by gen tox from a temperate phage

A

B

Exotoxin(Encoded by gen tox from a temperate phage)

Fragment B. Binding of the toxin

Fragment A. Enzymatic activity

slide20
Nicotinamide adenine dinucleotide phosphate (NAD)

Exotoxin

(A fragment)

ADP

Nicotinamide

Reaction with EF2

Protein synthesis

inhibition

ADP-EF2

testing immunity schick s test
Testing immunity(Schick’s test)
  • Intradermal injection (0.1 mL):

I. Cause inflammation (4-7 days later): No antitoxin in patient

II. No inflammation: Antitoxin is present (Immune person)

laboratory diagnosis
Laboratory diagnosis
  • Microscopic observation (differentiation from streptococcal and vansantnasopharyngitis)
  • Isolating the organism

Loffler’s medium

a tellurite plate

Tinsdal medium

  • Demonstrating toxin production

Animal inoculation

Eleck test

ELISA

  • PCR to detect tox gene
treatment
Treatment
  • Tracheostomyin children (to prevent croup)
  • Antitoxin

20000-100000 unit (Intra muscular)

  • Penicillin or erythromycin
prevention
Prevention
  • Vaccination

A combination of diphtheria toxoid, tetanus toxoid, and killed pertusis organism.

Given at 2, 4 an 6 months of age, with a booster at 1 and 6 years of age and then each 10 years afterward. (DPT or DT)

The toxoid is prepared by treating the exotoxin with 0.3% formaldehyde.

listeria monocytogenes
Listeria monocytogenes
  • Small rod like “chinese character”
  • No capsule, Facultative aerobic.
  • Tumbling movement. Movement in 25 c
  • Growing in 4c
  • Small and smooth colony on blood with a narrow zone of beta-hemolysis
  • Biochemical tests: Fermentation, Catalase + Oxidase +
disease
Disease
  • Meningitis and sepsis in
  • The fetus or newborn as a result of transmission across the placenta or during delivery.
  • Immunosuppressed adults
  • (especially renal transplant patients)
  • The infected mother: asymptomatic or influenzalike illness/ Abortion
transmission1
Transmission
  • The organism is distributed worldwide in animals, plants and soil.
  • Transmission to human by contact with animals or their feces

unpasteurized milk

contaminated vegetables.

Endogenously from gasterointestinal tract.

pathogenesis1
Pathogenesis

E-cadherin

Phagocytosis

into

epithelial cells

Internalin

Forming filopods

Phagolysosome formation

(acidic condition)

Inducing actin polymerization in cytoplasm

Phagocytiosis

By

macrophages

and hepatocytes

LysteriolysinO

secretion

Release from phagolysosome

lab diagnosis
Lab. diagnosis
  • Microscopic observation: Diphtheroids
  • Isolation by culture:

Blood and CSF samples on blood agar

Colonies: Small, gray colonies with a narrow zone of beta hemolysis

treatment1
Treatment
  • Penicillin

Resistant are rare

Prevention

  • Cell-mediated immunity is active but no immunization
  • Limiting the exposure of immunosuppressed patients to potential sources
spore forming gram positive bacilli
Spore-forming gram-positive bacilli
  • Bacillus (Aerobic)

B. antheracis, B.cereus

  • Clostridum (Anaerobic)

C. tetani, C. botulinum, C. perfringens, C. difficile

bacillus anthracis
Bacillus anthracis
  • Disease

Anthrax (common in animal but rare in humans).

properties1
Properties
  • A large rod with square ends.
  • Frequently in chains
  • A unique anti-phagocytic capsule is composed of D-glutamate.
  • Non-motile (other members of the genus are motile.)
transmission2
Transmission
  • Spores persist in soil for years. Infection from animal products (hides, bristles and wool), contact with sick animal.
  • Portals of entry: skin, mucous membranes, and respiratory tract.
clinical findings
Clinical findings
  • A typical lesion: A painless ulcer with black, necrotic eschar. Local edema.
  • Untreated cases progress to bacteremia and death.
  • Woolsorter’s disease (pulmonary anthrax) is a life threatening pneumonia (by inhalation of spores).
pathogenesis2
Pathogenesis
  • Invasiveness
  • Exotoxin
  • Anthrax toxin, has 3 components:
  • Protective antigen
  • Lethal factor: In the presence of protective antigen is rapidly fatal for mice. The action is unknown
  • Edema factor (an exotoxin): An adenylatecyclase dependent on protective antigen for its binding and entry into the cell.
lab diagnosis1
Lab. diagnosis
  • Samples: Exudate, Blood, sputum.
  • Direct smear: Large rods in chains. Spores not seen in smears of exudate.
  • Culture and biological/biochemical tests (Sensitivity to penicillin (String of pearls test), Fermentation, gelatin hydrolysis, Motility)
  • No serological tests are useful
prevention1
Prevention
  • Preventing soil contamination
  • Sterilizing dead animals and animal products .
  • Protecting persons at risk of exposure with special clothes.
  • Vaccination with cell-free vaccine for persons at high risk.
treatment2
Treatment
  • Penicillin

No resistant strain isolated

bacillus cereus
Bacillus cereus
  • Motile
  • No capsule
  • Saprophyte
bacillus cereus1
Bacillus cereus
  • Disease

Food poisoning

Rare infections: Meningitis, Osteomyelitis, …

  • Transmission

Spores on grains survive during steaming and rapid frying. Spore germinated when rice is kept warm.

Portal of entry is the gastrointestinal tract.

pathogenesis3
Pathogenesis
  • B. cereus produces 2 enterotoxins. Their actions is unclear.

Clinical findings

  • Emetic syndrome

A short incubation period (4 hours) with nausea and vomiting similar to staphylococcal food poisoning.

  • Diarrheal syndrome

Involves a long incubation period (18 hours) with diarrhea and resembles clostridial gastroenteritis.

lab diagnosis2
Lab. diagnosis
  • Not usually done

Treatment

No antibiotic is given. Only symptomatic treatment

Prevention

Grains (specially rice) should not be reheated

clostridiums
Clostridiums

An aerobic bacteria

Clostridiums tetani

Peritricus flagella

Terminal spore

  • Disease

Tetanus (Lockjaw)

clinical findings1
Clinical findings
  • Incubation period: 4-5 days – several weeks
  • Violent muscle spasms in the site of infection and then jaw)
  • Lockjaw (trismus) due to rigid contraction of the jaw muscles, which prevents the mouth from opening: a characteristic known as “risus sardonicus”’.
  • Low blood pressure
  • Respiratory failure
transmission3
Transmission

Spores are widespread in soil.

The portal of entry is a wound site.

Germination of spores is favoured by necrotic tissue and poor blood supply in the wound.

pathogenesis4
Pathogenesis
  • Tetanus toxin (tetanospasmin)

It is carried intra-axonally (retrograde) to the central nervous system, where it binds to ganglioside receptors and blocks release of inhibitory mediators (e.g. glycine, Gamma-aminobutiric acid) at spinal synapses leading to hyper reflection and spastic paralysis.

diagnosis
Diagnosis
  • History of wound and clinical picyure
  • There is no microbiologic or serologic diagnosis.
  • Organisms are rarely isolated from the wound site.

Treatment

  • Antitoxin does have a low effect
  • Penicillin
  • Respiratory support
  • Muscle relaxants
prevention2
Prevention
  • Immunization with toxoid in childhood (2, 4, 6, 12 months ages) and every 10 years thereafter.
  • When trauma occurs deeply:

1. Wound should be cleaned and debrided.

2. Tetanus toxoid booster should be given.

3. Tetanus immune globulin should be given.

4. Penicillin administered.

clostridium botulinum

Clostridium botulinum

Disease

Transmission

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment

Prevention

transmission4
Transmission
  • In soil ---> Alkaline vegetables/meat ---> canned/vacuum-packed ---> Spore germination ---> Toxin production ---> ingestion
pathogenesis5
Pathogenesis
  • Botulinus toxin

Observing from the gut ---> Carrying via the blood to peripheral nerve synapses ---> Blocking release of acetylcholine ---> Paralysis

clostridium perfringens
Clostridium perfringens
  • Disease: Gas Gangrene / Food Poisoning
  • Transmission
  • Pathogenesis
  • Clinical findings
  • Laboratory diagnosis
  • Treatment
  • Prevention
transmission5
Transmission
  • Soil, vegetative cells are members of normal flora in colon and vagina.
  • Is associated with war wounds.
pathogenesis and clinical findings
Pathogenesis and clinical findings
  • Alpha toxin: Lecithinase
  • Glycogen metabolism: Gas in tissues: Crepitation
  • Treatment

Penicillin

Wounds should be debrided

H2O2

lab diagnosis3
Lab diagnosis
  • Smear of tissue and exudate samples: large positive rods.
  • Cultured anaerobically identified with fermentation reactions
food poisoning
Food poisoning
  • Transmission: Soil and food. Survives cooking and grows to large numbers in reheated food, especially meat.
  • Pathogenesis: An enterotoxin (a protein in the spore coat)
  • Clinical findings:

Incubation: 8-16 hours, then watery diarrhea with cramps and little vomiting. Resolves in 24 hours.

treatment and prevention
Treatment and prevention
  • Treatment: Symptomatic – No antimicrobial drugs
  • Prevention: cooking well
clostridium difficile
Clostridium difficile

Disease

Transmission

Pathogenesis

Clinical Finding

Laboratory diagnosis

Treatment

Prevention

disease1
Disease
  • Antibiotic-associated pseudomembranous colitis

Transmission

It is a part of normal flora of gasterointestinal tract (3%)

pathogenesis6
Pathogenesis
  • Antibiotic (Clindamycin and ampicillin) supress drug-sensitive normal flora, allowing C. difficile to multiply: produce toxin.
  • Toxin mechanism is unclear
clinical findings2
Clinical findings
  • Diarrhea
  • Pseudomembranes (yellow-white plaques) on the colonic mucosa.
  • Visualised by sigmoidoscopy.
lab diagnosis4
Lab diagnosis
  • Toxin detectable in stool affecting on cell cultured cells.
  • Inhibition of cytotoxicity by specific antibody.
treatment3
Treatment
  • Withdrew the antibiotic
  • Oral vancomycin instead along with fluids.